Pathophysiologic mechanism of cardiac dysfunction in experimentally induced heartworm caval syndrome in dogs: An echocardiographic study

SUMMARY In dogs with experimentally induced heartworm infection, the onset of caval syndrome ( cs ) was characterized by a murmur, loudest over the tricuspid valve, and a large worm mass in the right ventricular lumen detectable during diastole by use of M-mode echocardiography. Two-dimensional echocardiography indicated that the worm mass was located in the right atrium and venae cavae and was “flowing” into the right ventricle during rapid diastolic filling. Paradoxical septal motion and vigorous right ventricular cranial wall motion also were observed. Other echocardiographic changes included decreased size of the left atrium and ventricle, aortic root, and ratio of left-to-right ventricular diastolic luminal diameter, compared with values obtained 6 months after experimentally induced heartworm infection. Right ventricular end diastolic diameter increased considerably. Most echocardiographic indices of left ventricular function (fractional shortening, velocity of circumferential fiber shortening, ejection fraction, and preejection period) were not altered appreciably, but estimates of cardiac index and stroke volume were markedly decreased. Electrocardiography revealed ventricular and supraventricular premature complexes in 7 of the 8 dogs studied, evidence of right ventricular enlargement in 6 of the 8 dogs studied, and increased mean heart rate, compared with that measured 6 months after inoculation of infective larvae, before the onset of cs . Cardiac catheterization was performed in 3 dogs at the onset of cs . Severe pulmonary arterial and right ventricular hypertension and decreased cardiac index (compared with values obtained before inoculation) were observed. Evidence of right ventricular inflow obstruction was not detected. Mean aortic blood pressure decreased with the onset of cs , but right ventricular end diastolic pressure increased. On the basis of these findings, a pathophysiologic mechanism for heart failure associated with heartworm cs was proposed. It involved the combination of newly acquired tricuspid valvular insufficiency and preexistent pulmonary hypertension leading to right-sided heart failure. Subsequent unloading of the left ventricle was likely responsible for diminished cardiac output in the face of apparently normal left ventricular function.